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Capture myopathy in live-stranded cetaceans.

P Herráez1, A Espinosa de los Monteros, A Fernández

  • 1Department of Comparative Pathology, Instituto Universitario de Sanidad Animal, Facultad de Veterinaria, Universidad de Las Palmas de Gran Canaria, Arucas, Spain. pherraez@dmor.ulpgc.es

Veterinary Journal (London, England : 1997)
|November 14, 2012
PubMed
Summary
This summary is machine-generated.

Capture myopathy (CM) is a significant factor in the deaths of live-stranded cetaceans. This study confirms a clinicopathological syndrome similar to terrestrial CM contributes to stranding outcomes in marine mammals.

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Area of Science:

  • Veterinary Pathology
  • Marine Mammal Science
  • Wildlife Toxicology

Background:

  • Live-stranded cetaceans often die following human interaction and rescue attempts.
  • Capture myopathy (CM) is a recognized condition in terrestrial wildlife, characterized by muscle degeneration and shock.
  • The role of CM in marine mammal strandings, particularly after rescue, requires further investigation.

Purpose of the Study:

  • To investigate the clinicopathological findings in live-stranded cetaceans that died after human capture/rescue.
  • To determine if a syndrome comparable to capture myopathy (CM) in terrestrial wildlife occurs in stranded cetaceans.
  • To establish diagnostic criteria for CM in cetaceans, especially when macroscopic lesions are subtle.

Main Methods:

  • Necropsy of 51 live-stranded cetaceans over 12 years.
  • Histological examination of skeletal muscle (longissimus dorsi) and cardiac muscle.
  • Immunohistochemical assays for myoglobin and fibrinogen to confirm ante-mortem muscle damage.
  • Detection of oxidative stress marker HSP70 in kidney tissue.

Main Results:

  • 25 out of 51 cetaceans exhibited lesions consistent with haemodynamic shock, muscle degeneration, and myoglobinuric nephrosis indicative of CM.
  • Histopathology revealed characteristic skeletal and cardiac muscle lesions, confirmed by immunohistochemistry.
  • All examined animals showed tubular nephrosis with myoglobin casts; HSP70 was present in tubular epithelium, suggesting oxidative stress.

Conclusions:

  • A clinicopathological syndrome comparable to capture myopathy (CM) significantly contributes to mortality in live-stranded cetaceans following rescue.
  • Subtle macroscopic lesions necessitate standardized histological and immunohistochemical diagnostic protocols for CM in cetaceans.
  • Understanding CM is crucial for improving outcomes for stranded marine mammals and informing rescue strategies.